Powell Amaranth (Amaranthus powellii) is a dicot weed in the Amaranthaceae family. In Ontario this weed first evolved multiple resistance (to 2 herbicide sites of action) in 1998 and infests Corn (maize), Soybean, and Wheat. Multiple resistance has evolved to herbicides in the Groups B/2, and C1/5. These particular biotypes are known to have resistance to atrazine, imazethapyr, and metribuzin and they may be cross-resistant to other herbicides in the Groups B/2, and C1/5.

The 'Group' letters/numbers that you see throughout this web site refer to the classification of herbicides by their site of action. To see a full list of herbicides and HRAC herbicide classifications click here.

We believe this case of multiple resistance is the result of sequential selection. The grower most
likely had triazine resistance in his fields in the 1980s.
Reliance on ALS inhibitors (mostly imazethapyr) increased in the 1990s and it is
very likely that this biotype was reselected for imazethapyr resistance.

Three grad students contributed on this biotype as part of their M. Sc. theses.
Gabrielle Ferguson did the initial work on this biotype, confirming ALS resistance.
Kris McNaughton was able to sequence the ALS gene and confirm the mutation.
SHane Diebold preformed the screen for ttriazine resistance and confirmed the presence of
the nuclear gene mutation.

Greenhouse, and Laboratory trials comparing a known susceptible Powell Amaranth biotype with this Powell Amaranth biotype have been used to confirm resistance. For further information on the tests conducted please contact the local weed scientists that provided this information.

Genetics

Genetic studies on Group B, C1/2, 5 resistant Powell Amaranth indicate that the inheritance is determined by a two gene trait. There may be a note below or an article discussing the genetics of this biotype in the Fact Sheets and Other Literature

Mechanism of Resistance

Studies on the mechanism of resistance of multiple resistant Powell Amaranth from Ontario indicate that resistance is due to an altered target site. There may be a note below or an article discussing the mechanism of resistance in the Fact Sheets and Other Literature

Relative Fitness

Triazine resistant weeds often exhibit a lower relative fitness when compared to susceptible biotypes. The most common mutation conferring triazine resistance (Ser 264 to Gly mutation of the psbA gene) also causes a reduction in CO2 fixation, quantum yield, and seed and biomass production. There is no record in this database referring specifically to fitness studies on multiple resistant Powell Amaranth from Ontario.

The Herbicide Resistance Action Committee, The Weed Science Society of America, and weed scientists in Ontario have been instrumental in providing you this information. Particular thanks is given to Francois Tardif for providing detailed information.

A previously unknown glyphosate resistance mechanism, amplification of the 5-enolpyruvyl shikimate-3-phosphate synthase gene, was recently reported in Amaranthus palmeri. This evolved mechanism could introgress to other weedy Amaranthus species through interspecific hybridization, representing an avenue for acquisition of a novel adaptive trait. The objective of this study was to evaluate the potential for this glyphosate resistance trait to transfer via pollen from A. palmeri to five other weedy Amaranthus species (Amaranthus hybridus, Amaranthus powellii, Amaranthus retroflexus, Amaranthus spinosus, and Amaranthus tuberculatus). Field and greenhouse crosses were conducted using glyphosate-resistant male A. palmeri as pollen donors and the other Amaranthus species as pollen recipients. Hybridization between A. palmeri and A. spinosus occurred with frequencies in the field studies ranging from <0.01% to 0.4%, and 1.4% in greenhouse crosses. A majority of the A. spinosus × A. palmeri hybrids grown to flowering were monoecious and produced viable seed. Hybridization occurred in the field study between A. palmeri and A. tuberculatus (<0.2%), and between A. palmeri and A. hybridus (<0.01%). This is the first documentation of hybridization between A. palmeri and both A. spinosus and A. hybridus..

A population of Amaranthus powellii that had survived imazethapyr did not have any of the documented AHAS mutations causing resistance in this species in Ontario. The goal of this research was to confirm resistance in this population, determine its molecular basis and develop diagnostic tests. Whole plant dose-response experiments showed the resistant population had greater than 25-fold resistance to the selective agent imazethapyr at the whole plant level. Whole plant resistance to other herbicides ranged between 9-fold to flumetsulam and 85-fold to flucarbazone. This was confirmed at the enzyme level with resistance ranging between 25-fold to imazethapyr and 485-fold to thifensulfuron. AHAS from the resistant population had 16% higher specific activity than that of the susceptible population and it was also less sensitive to feedback inhibition by valine, leucine and isoleucine. Genomic DNA was extracted to PCR amplify and sequence the AHAS gene and to determine the applicability of diagnostic tests. Sequencing of the AHAS gene revealed a single point mutation of thymine1125 to guanine coding for an Asp376Glu substitution. Two different diagnostic tests, restriction fragment length polymorphism and PCR amplification of specific allele, were able to correctly identify the resistant population from the susceptible control and from other resistant populations. Although this mutation appears to confer higher resistance to pyrithiobac and flucarbazone, two herbicides not registered in Eastern Canada, it endows plants with enough protection to allow survival to imazethapyr, the main selective agent in Ontario..

A population of Amaranthus powellii that had survived imazethapyr did not have any of the documented AHAS mutations causing resistance in this species in Ontario. The goal of this research was to confirm resistance in this population, determine its molecular basis and develop diagnostic tests. Whole plant dose–response experiments showed the resistant population had greater than 25-fold resistance to the selective agent imazethapyr at the whole plant level. Whole plant resistance to other herbicides ranged between 9-fold to flumetsulam and 85-fold to flucarbazone. This was confirmed at the enzyme level with resistance ranging between 25-fold to imazethapyr and 485-fold to thifensulfuron. AHAS from the resistant population had 16% higher specific activity than that of the susceptible population and it was also less sensitive to feedback inhibition by valine, leucine and isoleucine. Genomic DNA was extracted to PCR amplify and sequence the AHAS gene and to determine the applicability of diagnostic tests. Sequencing of the AHAS gene revealed a single point mutation of thymine1125 to guanine coding for an Asp376Glu substitution. Two different diagnostic tests, restriction fragment length polymorphism and PCR amplification of specific allele, were able to correctly identify the resistant population from the susceptible control and from other resistant populations. Although this mutation appears to confer higher resistance to pyrithiobac and flucarbazone, two herbicides not registered in Eastern Canada, it endows plants with enough protection to allow survival to imazethapyr, the main selective agent in Ontario..

Resistance to acetohydroxyacid synthase inhibitors is very widespread worldwide and is generally due to various point mutations in the gene coding for the target enzyme. Rapid resistance confirmation is key for the proper management of resistance. We aimed at determining whether two DNA-based tests, PCR-RFLP and PCR amplification of specific alleles (PASA), could reliably identify common AHAS mutations in Amaranthus sp., and whether individual tests could be multiplexed. DNA was extracted from eight populations of Amaranthus powellii and Amaranthus retroflexus possessing four different resistance alleles. Gains or losses of endonuclease recognition sites due to the presence of resistance alleles allowed reliable detection of all alleles. PASA used an allele-specific primer with a 3′-terminal mismatch to wildtype DNA to selectively amplify a resistance allele. All four resistance alleles were efficiently identified with PASA. Both tests were multiplexed to allow more efficient identification of resistance and up to four distinct mutations could be revealed by a single test. Those tests were relatively easy to use, inexpensive and allowed quick identification of resistance..

We investigated the effect of a herbicide resistance-conferring mutation on fitness in Amaranthus powellii. Morphological and histological observations were made. Growth and leaf appearance were recorded for six resistant and six susceptible populations. The competitiveness of a susceptible population was compared with that of a resistant population using a replacement series experiment. Leaves of the resistant plants were distorted and much smaller than those of susceptible plants. Additionally, they exhibited an abnormal morphological and structural pattern consisting of a mosaic of heterogeneous areas in the same leaf blade. The roots and stems had similar structures in susceptible and resistant plants, but the former were up to four times more developed. The resistant plants were slower to develop and produced 67% less biomass and 58% lower leaf area than susceptible plants. Under competitive conditions, one susceptible population outperformed one resistant population by 7-15 times. The Trp574Leu acetohydroxyacid synthase (AHAS) mutation appears to have considerable pleiotropic effects on the early growth and development of the plants which, in competitive conditions, greatly reduce fitness..